The most common form of Type 1 diabetes mellitus (T1DM) is an immune-mediated disease where insulin-secreting β-cells are destroyed by an autoimmune response. There are a number of genetic and environmental factors associated with the onset of the disease, which involves the progressive inflammatory infiltration of pancreatic islets containing immunocytes targeted specifically to insulin-secreting β-cells. This pathology develops over an indeterminate period of time (months to years). While the discovery of insulin allowed for the treatment of T1DM, there is currently no cure. The most common form of Type 1 diabetes mellitus is immune-mediated, in which insulin-producing β cells are destroyed. Yet, at the time of diagnosis, most patients still have appreciable amounts of insulin production. Preservation of residual β-cell function is highly desirable because it can reduce short-term and long-term complications of the disease.
Several clinical trials have been undertaken in an attempt to arrest autoimmunity in Type 1 diabetes with immunomodulatory agents or antigen-based treatments. Most notably, trials of anti-CD3, anti-CD20, and a GAD-65 antigen vaccine have shown some efficacy in preservation of β-cell function as evidenced by stimulated C-peptide secretion. T cells play a central part in autoimmunity associated with Type 1 diabetes.
However, there is need for additional new therapies for Type 1 diabetes mellitus that are able to halt or slow autoimmune β-cell destruction leading to preservation of β-cell function and C-peptide secretion, particularly in patients recently diagnosed with Type 1 diabetes.